Atherosclerosis (AS) is a chronic inflammatory vascular disease and the main pathological basis for numerous cardiovascular and cerebrovascular diseases. The pathogenesis of AS is complex and not yet fully elucidated. Vascular smooth muscle cells (VSMCs) are one of the main cell types that constitute the vascular wall. They are involved in regulating the systolic and diastolic functions of the vascular wall and maintaining the vascular tone. However, under the stimulation of AS promoting factors, the phenotypic switch occurs in systolic VSMCs, exhibiting characteristics such as proliferation, migration, adhesion, and calcification, which may directly lead to the formation or rupture of AS plaques. Integrins play a critical role in coordinating the transmembrane connections between the extracellular matrix and cytoskeleton, contributing to pathological processes of various diseases. They also play key roles in regulating the transdifferentiation of VSMCs into mesenchymal stem cells, myofibroblasts, macrophages, osteoblasts, and other cell types. To conclude, integrins can indirectly affect the formation and progression of AS by regulating the phenotypic transformation of VSMC, thereby presenting the potential as a new therapeutic target for AS. In this article, we review the classification of VSMC phenotypic transformation and the regulatory role of integrins in VSMC phenotypic transformation, aiming to provide new targets and strategies for the early treatment and intervention of AS.